Ask about this productRelated genes to: OSGIN1 antibody
- Gene:
- OSGIN1 NIH gene
- Name:
- oxidative stress induced growth inhibitor 1
- Previous symbol:
- -
- Synonyms:
- BDGI, OKL38
- Chromosome:
- 16q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2006-10-05
- Date modifiied:
- 2014-11-19
Related products to: OSGIN1 antibody
Related articles to: OSGIN1 antibody
- To identify oxidative stress (OS)-related genes involved in type 2 diabetes mellitus (T2DM) and screen potential Traditional Chinese Medicine (TCM) candidates for therapeutic use. - Source: PubMed
Jingnan H UMan LiaoZhongwen X IJing SongYining WangTao H E - Liver kinase B1 (LKB1) deficiency confers primary resistance to immune checkpoint inhibitors (ICIs) in non-small cell lung cancer; however, the underlying mechanisms remain unclear. Through single-cell RNA sequencing analysis of a genetically engineered Kras-driven mouse model with a conditional Lkb1 knockout, we discovered that LKB1-deficient tumors display dysregulation of the ferroptosis pathway. Analyses of multiple clinical cohorts revealed that LKB1-deficient lung tumors exhibit elevated ferroptosis resistance scores, which contribute to immunotherapy failure. Subsequent in vitro and in vivo experiments have shown that the deficiency of LKB1 hinders cellular susceptibility to ferroptosis induction, a situation that can be rectified by radiotherapy through DNMT1-dependent OSGIN1 downregulation. Concurrently, radiotherapy leads to the revival of stimulator of interferon genes (STING) expression, thereby triggering the activation of the immune microenvironment in LKB1-deficient lung tumors. The combination of radiotherapy with anti-PD-1 antibodies represents an effective, tailored therapeutic strategy in an LKB1-deficient murine model, resulting in significant tumor suppression through a ferroptosis-dependent mechanism. Collectively, the findings demonstrate that LKB1 deficiency promotes ferroptosis resistance in lung cancer cells. Radiotherapy simultaneously disrupts ferroptosis tolerance through the DNMT1-OSGIN1 axis and activates the STING pathway, effectively reversing ICI resistance in LKB1-deficient lung tumors. - Source: PubMed
Publication date: 2026/02/19
Zhang Yan-PeiWu Fei-FeiWu Ze-NanLi YanChen Jia-QiCai Xiao-TingQuan Xin-YiRong Zi-XuanGuo Ze-QinDuan Zhi-JiaoDong Zhong-YiGou Lan-YingZheng Da-YongWu De-Hua - Acute myeloid leukemia (AML) is one of the hematologic malignancies with a poor outcome. AML has a unique metabolic status, and identifying its metabolic vulnerabilities is warranted. Recent genome-wide screenings suggest that heme synthesis might be such a vulnerability. Heme is required not only for hemoglobin synthesis but also for the proper function of hemoproteins. Cytochromes are such hemoproteins and are necessary for mitochondrial respiration. Therefore, heme synthesis inhibition can diminish AML by altering mitochondrial status and function. However, still little is known about the importance of heme synthesis in leukemia cells. To reveal the roles of heme synthesis in leukemia, we treated human leukemia cell lines with heme synthesis inhibitors, succinylacetone (SA) or N-methyl protoporphyrin IX (NMPP). Heme synthesis inhibition induced cell growth inhibition and cell death in a concentration-dependent manner. Therefore, heme synthesis is required for leukemia cell proliferation and survival. Increased proapoptotic factors (cleaved caspase 3 and cleaved PARP) and decreased antiapoptotic factor (XIAP) were observed following heme synthesis inhibition. Cytochrome c and Smac were released into the cytoplasm by heme synthesis inhibition, suggesting that heme synthesis inhibition led to mitochondrial outer membrane permeabilization and activation of the intrinsic pathway of apoptosis. Comprehensive transcriptomic analysis revealed that heme synthesis inhibition induced OSGIN1 expression, leading to the release of cytochrome c and Smac from mitochondria into the cytoplasm. Therefore, heme synthesis inhibition induced leukemia apoptosis by activating the intrinsic apoptosis pathway. - Source: PubMed
Publication date: 2026/02/13
Yan YanKato HirokiSano SayakaFurukawa EijiroIchikawa SatoshiOnodera KoichiOnishi YasushiFukuhara NorikoYokoyama HisayukiFujiwara TohruHarigae Hideo - Curcumin, a polyphenolic compound derived from the plant Curcuma longa L., has demonstrated a wide range of therapeutic properties, including potential anticancer effects. However, its clinical efficacy is limited due to poor bioavailability and stability. To overcome these challenges, curcumin analogs like EF-24 have been developed with improved pharmacological properties. In this study, in order to improve our understanding of EF-24's potential mechanisms of action, we used whole-transcriptome sequencing to identify genome-wide functional impacts of EF-24 treatment in leukemia cells. These results enabled the development of a testable model system for associating druggable genes with clinical disease targets related to EF-24 treatment. To develop our model of the transcriptional response to EF-24 treatment, we used four well studied model cell lines for leukemia research, specifically the chronic myeloid leukemia (CML) cell line K-562 and acute myeloid leukemia (AML) cell lines HL-60, Kasumi-1, and THP-1. Cell viability was significantly decreased in all four of these leukemia models following EF-24 treatment as compared to untreated controls. We discovered that the genes ATF3, CLU, HSPA6, OSGIN1, ZFAND2A, and CXCL8, which are associated with reduced cell viability and proliferation, were consistently upregulated in all EF-24-treated cell lines. Further analysis of the tested cell lines revealed the activation of various signaling pathways, but notably the S100 family signaling pathway was consistently activated in all four cell lines. Our results provide critical insights into the molecular underpinnings of EF-24's antitumor efficacy against leukemia subtypes, highlighting its multifaceted impact on signaling pathways and gene networks that regulate cell survival, proliferation, and immune responses in cell line models of myeloid leukemia subtypes. - Source: PubMed
Publication date: 2025/09/23
Singh Ajeet PWax NoahDuncan JamesFernandes Ana SJacobs Jonathan L - Hepatocellular carcinoma is the most prevalent form of liver cancer worldwide and has high mortality rates. miRNAs, particularly miR-184, have been implicated in cancer biology, where they regulate gene expression and influence tumorigenesis. This study explored the role of miR-184 in HCC, revealing its dual function as both an oncogene and a tumor suppressor, depending on the target genes. We highlight the regulatory effects of miR-184 on critical genes such as INPPL1, FOXO3a, MTSS, OSGIN1, and SOX7 and its impact on key signaling pathways, including the Wnt/β-catenin and JAK2/STAT3/AKT pathways. Dysregulation of miR-184 expression in HCC tissues compared with normal liver tissue was linked to increased proliferation, reduced apoptosis, and autophagy inhibition. Furthermore, miR-184 shows promise as a diagnostic and prognostic biomarker in HCC because of its altered expression in cancerous tissues and blood. Its regulation through circRNAs and lncRNAs such as lncRNA UCA1, circ_0004913, circ-0001141, circ-102,166, LINC00205, and SNHG11 adds a layer of complexity, challenging us to delve deeper into the intricate mechanisms of miR-184, positioning it as a crucial target for potential therapeutic intervention. - Source: PubMed
Publication date: 2025/07/16
Hosseinzadeh LeilaJalilian FereshtehKalhori Mohammad RezaAlibakhshi RezaKalhori Amir AliKarami Mohsen